Citation and License

Diagnostic Pathology 2013, 8:124
doi:10.1186/1746-1596-8-124

Published: 31 July 2013

Abstract

Background

The novel pandemic A (H1N1) pdm09 virus was first identified in Mexico in April 2009
and since then it spread worldwide over a short period of time. Although the virus
infection is generally associated with mild disease and a relatively low mortality,
it is projected that mutations in specific regions of the viral genome, especially
within the receptor binding domain of the haemagglutinin (HA) protein could result
in more virulent virus stains, leading to a more severe pathogenicity.

Methods

To monitor the genetic polymorphisms at position 222 of Haemagglutinin of influenza
A(H1N1)pdm09 viruses from both outpatients with mild influenza and individuals with
severe disease requiring hospitalization, during 2009–2010 and 2010–2011 seasons,
a sequence-based genotypic assessment of viral populations to understand the prevalence
of D222G mutation.

Results

The D222G was identified in clinical specimens from 3 out of 42 cases analyzed in
Tunisia with severe outcome (7%). Interestingly, in one fatal case out of four viruses
taken from fatal cases studied (25%). Also this mutation was found in one mild case
out of 8 mild cases studied (0.1%). D222E substitution was found in virus taken from
one patient with severe clinical syndrome (2%) out of 42 severe cases analyzed and
E374K substitution was found in two severe cases (4%) out of 42 severe cases studied.

Conclusions

A specific mutation in the viral haemagglutinin (D222G) was found in fatal, severe
and mild case. Further virological, clinical and epidemiological investigations are
needed to ascertain the role of this and other mutations that may alter the virulence
and transmissibility of the pandemic influenza A (H1N1)pdm09.